3258 PLK4 Antibody #3258

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产品详细参数如下>>>>

产品名称：PLK4 Antibody #3258
货号：3258
品牌：CST(cell signaling)
抗体来源：Rabbit
克隆类型： Polyclonal
规格：

No.	Size	Price
3258P	40 ul (4 western blots)	询价
3258S	100 ul (10 western blots)	询价

抗体应用：

Applications	Reactivity	Sensitivity	MW (kDa)	Source
W IF-IC	H M R Mk	Endogenous	95	Rabbit

Applications Key:  W=Western Blotting  IF-IC=Immunofluorescence (Immunocytochemistry)
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Mon key
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on sequence homology.
特异性/敏感度： PLK4 Antibody detects endogenous levels of total PLK4 protein.
来源及纯化方法： Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Cys458 of human PLK4. Antibodies were purified by peptide affinity chromatography.
抗体背景：

At least four distinct polo-like kinases exist in mammalian cells: PLK1, PLK2, PLK3, and PLK4/SAK (1). PLK1 apparently plays many roles during mitosis, particularly in regulating mitotic entry and exit. The mitosis promoting factor (MPF), cdc2/cyclin B1, is activated by dephosphorylation of cdc2 (Thr14/Tyr15) by cdc25C. PLK1 phosphorylates cdc25C at Ser198 and cyclin B1 at Ser133 causing translocation of these proteins from the cytoplasm to the nucleus (2-5). PLK1 phosphorylation of Myt1 at Ser426 and Thr495 has been proposed to inactivate Myt1, one of the kinases known to phosphorylate cdc2 at Thr14/Tyr15 (6). Polo-like kinases also phosphorylate the cohesin subunit SCC1, causing cohesin displacement from chromosome arms that allow for proper cohesin localization to centromeres (7). Mitotic exit requires activation of the anaphase promoting complex (APC) (8), a ubiquitin ligase responsible for removal of cohesin at centromeres, and degradation of securin, cyclin A, cyclin B1, Aurora A, and cdc20 (9). PLK1 phosphorylation of the APC subunits Apc1, cdc16, and cdc27 has been demonstrated in vitro and has been proposed as a mechanism by which mitotic exit is regulated (10,11).Substitution of Thr210 with Asp has been reported to elevate PLK1 kinase activity and delay/arrest cells in mitosis, while a Ser137Asp substitution leads to S-phase arrest (12). In addition, while DNA damage has been found to inhibit PLK1 kinase activity, the Thr210Asp mutant is resistant to this inhibition (13). PLK1 has been reported to be phosphorylated in vivo at Ser137 and Thr210 in mitosis; DNA damage prevents phosphorylation at these sites (14).

关键词：CST，抗体，一抗{byao_back}{byao_back2}

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